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3 Hemodynamics: Factors Affecting Blood Flow

3 Hemodynamics: Factors Affecting Blood Flow

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Transcytosis

A small quantity of material crosses capillary walls by transcyto¯ -sis; trans- ϭ across; -cyt- ϭ cell; -osis ϭ process).

sis (tranzЈ-sı¯-TO

In this process, substances in blood plasma become enclosed

within tiny pinocytic vesicles that first enter endothelial cells by

endocytosis, then move across the cell and exit on the other side

by exocytosis. This method of transport is important mainly for

large, lipid-insoluble molecules that cannot cross capillary walls

in any other way. For example, the hormone insulin (a small protein) enters the bloodstream by transcytosis, and certain antibodies (also proteins) pass from the maternal circulation into the fetal

circulation by transcytosis.



Bulk Flow: Filtration and Reabsorption

Bulk flow is a passive process in which large numbers of ions,

molecules, or particles in a fluid move together in the same direction. The substances move at rates far greater than can be accounted for by diffusion alone. Bulk flow occurs from an area of

higher pressure to an area of lower pressure, and it continues as

long as a pressure difference exists. Diffusion is more important

for solute exchange between blood and interstitial fluid, but bulk

flow is more important for regulation of the relative volumes of

blood and interstitial fluid. Pressure-driven movement of fluid

and solutes from blood capillaries into interstitial fluid is called

filtration. Pressure-driven movement from interstitial fluid into

blood capillaries is called reabsorption.

Two pressures promote filtration: blood hydrostatic pressure

(BHP), the pressure generated by the pumping action of the heart,

and interstitial fluid osmotic pressure (inЈ-ter-STISH-al). The

main pressure promoting reabsorption of fluid is blood colloid



osmotic pressure. The balance of these pressures, called net filtration pressure (NFP), determines whether the volumes of

blood and interstitial fluid remain steady or change. Overall, the

volume of fluid and solutes reabsorbed normally is almost as

large as the volume filtered. This near equilibrium is known as

Starling’s law of the capillaries. Let’s see how these hydrostatic

and osmotic pressures balance.

Within vessels, the hydrostatic pressure is due to the pressure

that water in blood plasma exerts against blood vessel walls.

The blood hydrostatic pressure (BHP) is about 35 millimeters

of mercury (mmHg) at the arterial end of a capillary, and about

16 mmHg at the capillary’s venous end (Figure 21.7). BHP

“pushes” fluid out of capillaries into interstitial fluid. The opposing pressure of the interstitial fluid, called interstitial fluid hydrostatic pressure (IFHP), “pushes” fluid from interstitial spaces

back into capillaries. However, IFHP is close to zero. (IFHP is difficult to measure, and its reported values vary from small positive

values to small negative values.) For our discussion we assume

that IFHP equals 0 mmHg all along the capillaries.

The difference in osmotic pressure across a capillary wall is

due almost entirely to the presence in blood of plasma proteins,

which are too large to pass through either fenestrations or gaps

between endothelial cells. Blood colloid osmotic pressure

(BCOP) is a force caused by the colloidal suspension of these

large proteins in plasma that averages 26 mmHg in most capillaries. The effect of BCOP is to “pull” fluid from interstitial

spaces into capillaries. Opposing BCOP is interstitial fluid osmotic pressure (IFOP), which “pulls” fluid out of capillaries

into interstitial fluid. Normally, IFOP is very small—0.1–

5 mmHg—because only tiny amounts of protein are present in

interstitial fluid. The small amount of protein that leaks from

blood plasma into interstitial fluid does not accumulate there

because it passes into lymph in lymphatic capillaries and is

eventually returned to the blood. For discussion, we can use a

value of 1 mmHg for IFOP.

Whether fluids leave or enter capillaries depends on the balance of pressures. If the pressures that push fluid out of capillaries

exceed the pressures that pull fluid into capillaries, fluid will

move from capillaries into interstitial spaces (filtration). If, however, the pressures that push fluid out of interstitial spaces into

capillaries exceed the pressures that pull fluid out of capillaries,

then fluid will move from interstitial spaces into capillaries (reabsorption).

The net filtration pressure (NFP), which indicates the direction

of fluid movement, is calculated as follows:

NFP ϭ (BHP ϩ IFOP) Ϫ (BCOP ϩ IFHP)

Pressures that

promote filtration



Pressures that

promote reabsorption



At the arterial end of a capillary,

NFP ϭ (35 ϩ 1) mmHg Ϫ (26 ϩ 0) mmHg

ϭ 36 Ϫ 26 mmHg ϭ 10 mmHg

Thus, at the arterial end of a capillary, there is a net outward

pressure of 10 mmHg, and fluid moves out of the capillary into

interstitial spaces (filtration).



21



Lipid-soluble materials, such as O2, CO2, and steroid hormones,

may pass across capillary walls directly through the lipid bilayer of

endothelial cell plasma membranes. Most plasma proteins and red

blood cells cannot pass through capillary walls of continuous and

fenestrated capillaries because they are too large to fit through the

intercellular clefts and fenestrations.

In sinusoids, however, the intercellular clefts are so large that

they allow even proteins and blood cells to pass through their

walls. For example, hepatocytes (liver cells) synthesize and release

many plasma proteins, such as fibrinogen (the main clotting protein) and albumin, which then diffuse into the bloodstream through

sinusoids. In red bone marrow, blood cells are formed (hemopoiesis) and then enter the bloodstream through sinusoids.

In contrast to sinusoids, the capillaries of the brain allow

only a few substances to move across their walls. Most areas of

the brain contain continuous capillaries; however, these capillaries are very “tight.” The endothelial cells of most brain capillaries are sealed together by tight junctions. The resulting

blockade to movement of materials into and out of brain capillaries is known as the blood–brain barrier (see Section 14.1).

In brain areas that lack the blood–brain barrier, for example,

the hypothalamus, pineal gland, and pituitary gland, materials

undergo capillary exchange more freely.



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C H A P T E R



21.2 CAPILLARY EXCHANGE



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CHAPTER 21



• THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS AND HEMODYNAMICS



Figure 21.7 Dynamics of capillary exchange (Starling’s law of the capillaries). Excess filtered fluid drains into lymphatic

capillaries.

Blood hydrostatic pressure pushes fluid out of capillaries (filtration), and blood colloid osmotic pressure pulls fluid into

capillaries (reabsorption).

Key:



Lymphatic fluid (lymph)

returns to

Blood plasma



Lymphatic

capillary



Tissue

cell



CLINICAL CONNECTION | Edema



Interstitial

fluid



Blood flow from arteriole

into capillary



IFOP =

1 mmHg



Blood flow from

capillary

into venule



IFHP =

0 mmHg

BHP =

BCOP =

35 mmHg 26 mmHg



BHP =

16 mmHg

BCOP =

26 mmHg



N

F

P



N

F

P



Net filtration at arterial end of

capillaries (20 liters per day)

Net filtration

pressure (NFP)



=



(BHP + IFOP)

Pressures promoting

filtration



Result



BHP = Blood hydrostatic pressure

IFHP = Interstitial fluid hydrostatic pressure

BCOP = Blood colloid osmotic pressure

IFOP = Interstitial fluid osmotic pressure

NFP = Net filtration pressure



• Increased capillary blood pressure causes

more fluid to be filtered from capillaries.

• Increased permeability of capillaries raises

interstitial fluid osmotic pressure by allowing some plasma proteins to escape. Such

leakiness may be caused by the destructive

effects of chemical, bacterial, thermal, or

mechanical agents on capillary walls.



Net reabsorption at venous end

of capillaries (17 liters per day)





(BCOP + IFHP)

Pressures promoting

reabsorption



Arterial end



Venous end



NFP = (35 + 1) – (26 + 0)

= 10 mmHg



NFP = (16 + 1) – (26 + 0)

= –9 mmHg



Net filtration



Net reabsorption



If filtration greatly exceeds reabsorption, the result is edema (e-DE¯-ma ϭ

swelling), an abnormal increase in interstitial fluid volume. Edema is not usually

detectable in tissues until interstitial fluid volume has risen to 30% above normal. Edema

can result from either excess filtration or inadequate reabsorption.

Two situations may cause excess filtration:



One situation commonly causes inadequate reabsorption:

• Decreased concentration of plasma proteins lowers the blood colloid osmotic

pressure. Inadequate synthesis or dietary

intake or loss of plasma proteins is associated with liver disease, burns, malnutrition

(for example, kwashiorkor; see Disorders:

Homeostatic Imbalances in Chapter 25),

and kidney disease. •



A person who has liver failure cannot synthesize the normal amount of plasma proteins. How does a deficit of plasma

proteins affect blood colloid osmotic pressure, and what is the effect on capillary exchange?



At the venous end of a capillary,

NFP ϭ (16 ϩ 1) mmHg Ϫ (26 ϩ 0) mmHg

ϭ 17 Ϫ 26 mmHg ϭ Ϫ9 mmHg

At the venous end of a capillary, the negative value (Ϫ9 mmHg)

represents a net inward pressure, and fluid moves into the capillary from tissue spaces (reabsorption).

On average, about 85% of the fluid filtered out of capillaries is

reabsorbed. The excess filtered fluid and the few plasma proteins that

do escape from blood into interstitial fluid enter lymphatic capillaries

(see Figure 22.2). As lymph drains into the junction of the jugular



and subclavian veins in the upper thorax (see Figure 22.3), these

materials return to the blood. Every day about 20 liters of fluid

filter out of capillaries in tissues throughout the body. Of this

fluid, 17 liters are reabsorbed and 3 liters enter lymphatic capillaries (excluding filtration during urine formation).

CHECKPOINT



6. How can substances enter and leave blood plasma?

7. How do hydrostatic and osmotic pressures determine

fluid movement across the walls of capillaries?

8. Define edema and describe how it develops.



21.3 HEMODYNAMICS: FACTORS AFFECTING BLOOD FLOW



Figure 21.8 Blood pressures in various parts of the

cardiovascular system. The dashed line is the mean (average)

blood pressure in the aorta, arteries, and arterioles.



OBJECTIVES



Blood pressure rises and falls with each heartbeat in

blood vessels leading to capillaries.



• Explain the factors that regulate the volume of blood

flow.

• Explain how blood pressure changes throughout the

cardiovascular system.

• Describe the factors that determine mean arterial pressure

and systemic vascular resistance.

• Describe the relationship between cross-sectional area and

velocity of blood flow.



MAP ϭ diastolic BP ϩ 1͞3 (systolic BP Ϫ diastolic BP)



80



60

Diastolic blood

pressure



40



20



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0



Is the mean blood pressure in the aorta closer to systolic

or to diastolic pressure?



Thus, in a person whose BP is 110/70 mmHg, MAP is about

83 mmHg [70 ϩ 1/3(110 Ϫ 70)].

We have already seen that cardiac output equals heart rate multiplied by stroke volume. Another way to calculate cardiac output

is to divide mean arterial pressure (MAP) by resistance (R):

CO ϭ MAP Ϭ R. By rearranging the terms of this equation, you

can see that MAP ϭ CO ϫ R. If cardiac output rises due to an

increase in stroke volume or heart rate, then the mean arterial

pressure rises as long as resistance remains steady. Likewise, a

decrease in cardiac output causes a decrease in mean arterial pressure if resistance does not change.

Blood pressure also depends on the total volume of blood in

the cardiovascular system. The normal volume of blood in an

adult is about 5 liters (5.3 qt). Any decrease in this volume, as

from hemorrhage, decreases the amount of blood that is circulated through the arteries each minute. A modest decrease can

be compensated for by homeostatic mechanisms that help

maintain blood pressure (described in Section 21.4), but if the

decrease in blood volume is greater than 10% of the total, blood

pressure drops. Conversely, anything that increases blood volume, such as water retention in the body, tends to increase

blood pressure.



21



As you have just learned, blood flows from regions of higher pressure to regions of lower pressure; the greater the pressure difference,

the greater the blood flow. Contraction of the ventricles generates

blood pressure (BP), the hydrostatic pressure exerted by blood on

the walls of a blood vessel. BP is determined by cardiac output (see

Section 20.5), blood volume, and vascular resistance (described

shortly). BP is highest in the aorta and large systemic arteries; in a

resting, young adult, BP rises to about 110 mmHg during systole

(ventricular contraction) and drops to about 70 mmHg during diastole (ventricular relaxation). Systolic blood pressure (SBP) (sisTOL-ik) is the highest pressure attained in arteries during systole,

and diastolic blood pressure (DBP) (dı¯-a-STOL-ik) is the lowest

arterial pressure during diastole (Figure 21.8). As blood leaves the

aorta and flows through the systemic circulation, its pressure falls

progressively as the distance from the left ventricle increases. Blood

pressure decreases to about 35 mmHg as blood passes from systemic arteries through systemic arterioles and into capillaries, where

the pressure fluctuations disappear. At the venous end of capillaries,

blood pressure has dropped to about 16 mmHg. Blood pressure continues to drop as blood enters systemic venules and then veins because these vessels are farthest from the left ventricle. Finally, blood

pressure reaches 0 mmHg as blood flows into the right ventricle.

Mean arterial pressure (MAP), the average blood pressure in

arteries, is roughly one-third of the way between the diastolic and

systolic pressures. It can be estimated as follows:



100



C H A P T E R



Blood Pressure



Systolic blood

pressure



120



Pressure (mmHg)



Blood flow is the volume of blood that flows through any tissue

in a given time period (in mL/min). Total blood flow is cardiac

output (CO), the volume of blood that circulates through systemic (or pulmonary) blood vessels each minute. In Chapter 20

we saw that cardiac output depends on heart rate and stroke volume: Cardiac output (CO) ϭ heart rate (HR) ϫ stroke volume

(SV). How the cardiac output becomes distributed into circulatory routes that serve various body tissues depends on two more

factors: (1) the pressure difference that drives the blood flow

through a tissue and (2) the resistance to blood flow in specific

blood vessels. Blood flows from regions of higher pressure to

regions of lower pressure; the greater the pressure difference,

the greater the blood flow. But the higher the resistance, the

smaller the blood flow.



140



te



21.3 Hemodynamics: Factors

Affecting Blood Flow



741



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CHAPTER 21



• THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS AND HEMODYNAMICS



Vascular Resistance

As noted earlier, vascular resistance is the opposition to blood

flow due to friction between blood and the walls of blood vessels.

Vascular resistance depends on (1) size of the blood vessel lumen,

(2) blood viscosity, and (3) total blood vessel length.

1. Size of the lumen. The smaller the lumen of a blood vessel, the

greater its resistance to blood flow. Resistance is inversely

proportional to the fourth power of the diameter (d) of the

blood vessel’s lumen (R ϰ 1/d4). The smaller the diameter of

the blood vessel, the greater the resistance it offers to blood

flow. For example, if the diameter of a blood vessel decreases

by one-half, its resistance to blood flow increases 16 times.

Vasoconstriction narrows the lumen, and vasodilation widens

it. Normally, moment-to-moment fluctuations in blood flow

through a given tissue are due to vasoconstriction and vasodilation of the tissue’s arterioles. As arterioles dilate, resistance

decreases, and blood pressure falls. As arterioles constrict,

resistance increases, and blood pressure rises.

2. Blood viscosity. The viscosity (vis-KOS-i-te¯ ϭ thickness) of

blood depends mostly on the ratio of red blood cells to plasma

(fluid) volume, and to a smaller extent on the concentration of

proteins in plasma. The higher the blood’s viscosity, the higher

the resistance. Any condition that increases the viscosity of

blood, such as dehydration or polycythemia (an unusually

high number of red blood cells), thus increases blood pressure.

A depletion of plasma proteins or red blood cells, due to anemia or hemorrhage, decreases viscosity and thus decreases

blood pressure.

3. Total blood vessel length. Resistance to blood flow through a

vessel is directly proportional to the length of the blood vessel.

The longer a blood vessel, the greater the resistance. Obese

people often have hypertension (elevated blood pressure) because the additional blood vessels in their adipose tissue increase their total blood vessel length. An estimated 650 km

(about 400 miles) of additional blood vessels develop for each

extra kilogram (2.2 lb) of fat.

Systemic vascular resistance (SVR), also known as total

peripheral resistance (TPR), refers to all of the vascular resistances

offered by systemic blood vessels. The diameters of arteries and

veins are large, so their resistance is very small because most of

the blood does not come into physical contact with the walls of

the blood vessel. The smallest vessels—arterioles, capillaries, and

venules—contribute the most resistance. A major function of

arterioles is to control SVR—and therefore blood pressure and

blood flow to particular tissues—by changing their diameters.

Arterioles need to vasodilate or vasoconstrict only slightly to have

a large effect on SVR. The main center for regulation of SVR is

the vasomotor center in the brain stem (described shortly).



Venous Return

Venous return, the volume of blood flowing back to the heart

through the systemic veins, occurs due to the pressure generated by contractions of the heart’s left ventricle. The pressure



difference from venules (averaging about 16 mmHg) to the

right ventricle (0 mmHg), although small, normally is sufficient to cause venous return to the heart. If pressure increases

in the right atrium or ventricle, venous return will decrease.

One cause of increased pressure in the right atrium is an incompetent (leaky) tricuspid valve, which lets blood regurgitate

(flow backward) as the ventricles contract. The result is decreased venous return and buildup of blood on the venous side

of the systemic circulation.

When you stand up, for example, at the end of an anatomy and

physiology lecture, the pressure pushing blood up the veins in

your lower limbs is barely enough to overcome the force of gravity pushing it back down. Besides the heart, two other mechanisms “pump” blood from the lower body back to the heart: (1)

the skeletal muscle pump and (2) the respiratory pump. Both

pumps depend on the presence of valves in veins.

The skeletal muscle pump operates as follows (Figure 21.9):

1



While you are standing at rest, both the venous valve closer

to the heart (proximal valve) and the one farther from the

heart (distal valve) in this part of the leg are open, and blood

flows upward toward the heart.



Figure 21.9 Action of the skeletal muscle pump in returning

blood to the heart.

Milking refers to skeletal muscle contractions that drive

venous blood toward the heart.



Proximal

valve



Distal

valve



1



2



3



Aside from cardiac contractions, what mechanisms act as

pumps to boost venous return?



21.3 HEMODYNAMICS: FACTORS AFFECTING BLOOD FLOW

2



3



Contraction of leg muscles, such as when you stand on tiptoes or take a step, compresses the vein. The compression

pushes blood through the proximal valve, an action called

milking. At the same time, the distal valve in the uncompressed segment of the vein closes as some blood is pushed

against it. People who are immobilized through injury or disease lack these contractions of leg muscles. As a result, their

venous return is slower and they may develop circulation

problems.

Just after muscle relaxation, pressure falls in the previously

compressed section of vein, which causes the proximal valve

to close. The distal valve now opens because blood pressure

in the foot is higher than in the leg, and the vein fills with

blood from the foot. The proximal valve then reopens.



The respiratory pump is also based on alternating compression and decompression of veins. During inhalation, the diaphragm moves downward, which causes a decrease in pressure in

the thoracic cavity and an increase in pressure in the abdominal

cavity. As a result, abdominal veins are compressed, and a greater

volume of blood moves from the compressed abdominal veins

into the decompressed thoracic veins and then into the right

atrium. When the pressures reverse during exhalation, the valves

in the veins prevent backflow of blood from the thoracic veins to

the abdominal veins.



743



Figure 21.10 summarizes the factors that increase blood pressure

through increasing cardiac output or systemic vascular resistance.



CLINICAL CONNECTION | Syncope

Syncope (SIN-ko¯-pe¯), or fainting, is a sudden, temporary loss

of consciousness that is not due to head trauma, followed by

spontaneous recovery. It is most commonly due to cerebral

ischemia, lack of sufficient blood flow to the brain. Syncope may occur for several reasons:

• Vasodepressor syncope is due to sudden emotional stress or real,

threatened, or fantasized injury.

• Situational syncope is caused by pressure stress associated with

urination, defecation, or severe coughing.

• Drug-induced syncope may be caused by drugs such as antihypertensives, diuretics, vasodilators, and tranquilizers.

• Orthostatic hypotension, an excessive decrease in blood pressure

that occurs on standing up, may cause fainting. •



Velocity of Blood Flow

Earlier we saw that blood flow is the volume of blood that flows

through any tissue in a given time period (in mL/min). The

speed or velocity of blood flow (in cm/sec) is inversely related

to the cross-sectional area. Velocity is slowest where the total



Figure 21.10 Summary of factors that increase blood pressure. Changes noted within green boxes increase cardiac output;

changes noted within blue boxes increase systemic vascular resistance.

Increases in cardiac output and increases in systemic vascular resistance will increase mean arterial pressure.

Skeletal muscle pump



Respiratory

pump



Venoconstriction



Decreased

parasympathetic

impulses



Increased sympathetic

impulses and hormones

from adrenal medulla



Increased

heart rate

(HR)



Increased

stroke

volume (SV)



Increased

venous

return



Increased number

of red blood cells,

as in polycythemia



Increased

blood

viscosity



Increased cardiac

output (CO)



Increased

body size, as

in obesity



Increased

total blood

vessel length



Decreased blood

vessel radius

(vasoconstriction)



Increased systemic

vascular resistance (SVR)



Increased mean arterial

pressure (MAP)



Which type of blood vessel exerts the major control of systemic vascular resistance, and how does it achieve this?



C H A P T E R



21



Increased blood

volume



744



CHAPTER 21



• THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS AND HEMODYNAMICS



Figure 21.11 Relationship between velocity (speed) of blood

flow and total cross-sectional area in different types of blood

vessels.



11. How is the return of venous blood to the heart

accomplished?

12. Why is the velocity of blood flow faster in arteries and

veins than in capillaries?



Velocity of blood flow is slowest in the capillaries

because they have the largest total cross-sectional area.



21.4 Control of Blood Pressure

and Blood Flow

Cross-sectional

area



OBJECTIVE



• Describe how blood pressure is regulated.



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Velocity



Several interconnected negative feedback systems control

blood pressure by adjusting heart rate, stroke volume, systemic

vascular resistance, and blood volume. Some systems allow

rapid adjustments to cope with sudden changes, such as the

drop in blood pressure in the brain that occurs when you get out

of bed; others act more slowly to provide long-term regulation

of blood pressure. The body may also require adjustments to

the distribution of blood flow. During exercise, for example, a

greater percentage of the total blood flow is diverted to skeletal

muscles.



In which blood vessels is the velocity of flow fastest?



cross-sectional area is greatest (Figure 21.11). Each time an artery branches, the total cross-sectional area of all of its branches

is greater than the cross-sectional area of the original vessel, so

blood flow becomes slower and slower as blood moves further

away from the heart, and is slowest in the capillaries. Conversely,

when venules unite to form veins, the total cross-sectional area

becomes smaller and flow becomes faster. In an adult, the crosssectional area of the aorta is only 3–5 cm2, and the average velocity of the blood there is 40 cm/sec. In capillaries, the total

cross-sectional area is 4500–6000 cm2, and the velocity of blood

flow is less than 0.1 cm/sec. In the two venae cavae combined,

the cross-sectional area is about 14 cm2, and the velocity is

about 15 cm/sec. Thus, the velocity of blood flow decreases as

blood flows from the aorta to arteries to arterioles to capillaries,

and increases as it leaves capillaries and returns to the heart. The

relatively slow rate of flow through capillaries aids the exchange

of materials between blood and interstitial fluid.

Circulation time is the time required for a drop of blood to

pass from the right atrium, through the pulmonary circulation,

back to the left atrium, through the systemic circulation down to

the foot, and back again to the right atrium. In a resting person,

circulation time normally is about 1 minute.

CHECKPOINT



9. Explain how blood pressure and resistance determine

volume of blood flow.

10. What is systemic vascular resistance and what factors

contribute to it?



Role of the Cardiovascular Center

In Chapter 20, we noted how the cardiovascular (CV) center in

the medulla oblongata helps regulate heart rate and stroke volume. The CV center also controls neural, hormonal, and local

negative feedback systems that regulate blood pressure and blood

flow to specific tissues. Groups of neurons scattered within the

CV center regulate heart rate, contractility (force of contraction)

of the ventricles, and blood vessel diameter. Some neurons stimulate the heart (cardiostimulatory center); others inhibit the heart

(cardioinhibitory center). Still others control blood vessel diameter by causing constriction (vasoconstrictor center) or dilation

(vasodilator center); these neurons are referred to collectively as

the vasomotor center. Because the CV center neurons communicate with one another, function together, and are not clearly separated anatomically, we discuss them here as a group.

The cardiovascular center receives input both from higher

brain regions and from sensory receptors (Figure 21.12). Nerve

impulses descend from the cerebral cortex, limbic system, and

hypothalamus to affect the cardiovascular center. For example,

even before you start to run a race, your heart rate may increase

due to nerve impulses conveyed from the limbic system to the

CV center. If your body temperature rises during a race, the hypothalamus sends nerve impulses to the CV center. The resulting vasodilation of skin blood vessels allows heat to dissipate

more rapidly from the surface of the skin. The three main types

of sensory receptors that provide input to the cardiovascular

center are proprioceptors, baroreceptors, and chemoreceptors.

¯ -pre¯-o¯-sepЈ-tors) monitor movements of

Proprioceptors (PRO

joints and muscles and provide input to the cardiovascular center during physical activity. Their activity accounts for the rapid

increase in heart rate at the beginning of exercise. Baroreceptors

(barЈ-o¯-re¯-SEP-tors) monitor changes in pressure and stretch in



21.4 CONTROL OF BLOOD PRESSURE AND BLOOD FLOW



the walls of blood vessels, and chemoreceptors (ke¯Ј-mo¯-re¯SEP-tors) monitor the concentration of various chemicals in the

blood.

Output from the cardiovascular center flows along sympathetic

and parasympathetic neurons of the ANS (Figure 21.12). Sympathetic impulses reach the heart via the cardiac accelerator

nerves. An increase in sympathetic stimulation increases heart

rate and contractility; a decrease in sympathetic stimulation decreases heart rate and contractility. Parasympathetic stimulation,

conveyed along the vagus (X) nerves, decreases heart rate. Thus,

opposing sympathetic (stimulatory) and parasympathetic (inhibitory) influences control the heart.

The cardiovascular center also continually sends impulses to

smooth muscle in blood vessel walls via vasomotor nerves (va¯¯ -tor). These sympathetic neurons exit the spinal cord

soˉ-MO

through all thoracic and the first one or two lumbar spinal nerves

and then pass into the sympathetic trunk ganglia (see Figure 15.2).

From there, impulses propagate along sympathetic neurons that

innervate blood vessels in viscera and peripheral areas. The vasomotor region of the cardiovascular center continually sends impulses over these routes to arterioles throughout the body, but especially to those in the skin and abdominal viscera. The result is a

moderate state of tonic contraction or vasoconstriction, called

vasomotor tone, that sets the resting level of systemic vascular

resistance. Sympathetic stimulation of most veins causes constriction that moves blood out of venous blood reservoirs and

increases blood pressure.



745



Neural Regulation of Blood Pressure

The nervous system regulates blood pressure via negative feedback loops that occur as two types of reflexes: baroreceptor

reflexes and chemoreceptor reflexes.



Baroreceptor Reflexes

Baroreceptors, pressure-sensitive sensory receptors, are located

in the aorta, internal carotid arteries (arteries in the neck that supply blood to the brain), and other large arteries in the neck and

chest. They send impulses to the cardiovascular center to help

regulate blood pressure. The two most important baroreceptor

reflexes are the carotid sinus reflex and the aortic reflex.

Baroreceptors in the wall of the carotid sinuses initiate the

carotid sinus reflex (ka-ROT-id), which helps regulate blood

pressure in the brain. The carotid sinuses are small widenings of

the right and left internal carotid arteries just above the point

where they branch from the common carotid arteries (Figure 21.13).

Blood pressure stretches the wall of the carotid sinus, which

stimulates the baroreceptors. Nerve impulses propagate from the

carotid sinus baroreceptors over sensory axons in the glossopharyngeal (IX) nerves (glosЈ-o¯-fa-RIN-je¯-al) to the cardiovascular

center in the medulla oblongata. Baroreceptors in the wall of the

ascending aorta and arch of the aorta initiate the aortic reflex,

which regulates systemic blood pressure. Nerve impulses from

aortic baroreceptors reach the cardiovascular center via sensory

axons of the vagus (X) nerves.



Figure 21.12 Location and function of the cardiovascular (CV) center in the medulla oblongata. The CV center receives

input from higher brain centers, proprioceptors, baroreceptors, and chemoreceptors. Then, it provides output to the

sympathetic and parasympathetic divisions of the autonomic nervous system (ANS).



INPUT TO CARDIOVASCULAR

CENTER (nerve impulses)

From higher brain centers: cerebral cortex,

limbic system, and hypothalamus

From proprioceptors: monitor joint movements

From baroreceptors: monitor blood pressure

From chemoreceptors: monitor blood acidity

+

(H ), CO2, and O2



Vagus nerves

(parasympathetic)

Cardiac accelerator



OUTPUT TO EFFECTORS

(increased frequency of nerve impulses)

Heart: decreased rate



Heart: increased rate and contractility



nerves (sympathetic)

CARDIOVASCULAR

(CV) CENTER



Vasomotor nerves

(sympathetic)



What types of effector tissues are regulated by the cardiovascular center?



Blood vessels: vasoconstriction



C H A P T E R



21



The cardiovascular center is the main region for nervous system regulation of the heart and blood vessels.



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CHAPTER 21



• THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS AND HEMODYNAMICS



Figure 21.13 ANS innervation of the heart and the baroreceptor reflexes that help regulate blood pressure.

Baroreceptors are pressure-sensitive neurons that monitor stretching.



Baroreceptors

in carotid sinus

Glossopharyngeal (IX) nerves

Baroreceptors

in arch of aorta



Cardiovascular

(CV) center



Medulla oblongata



Vagus (X) nerves,

parasympathetic

SA node

AV node



Ventricular

myocardium



Spinal cord



Key:

Sensory (afferent) neurons

Motor (efferent) neurons



Cardiac accelerator

nerve (sympathetic)

Sympathetic trunk

ganglion



Which cranial nerves conduct impulses to the cardiovascular center from baroreceptors in the carotid sinuses and

the arch of the aorta?



When blood pressure falls, the baroreceptors are stretched less,

and they send nerve impulses at a slower rate to the cardiovascular center (Figure 21.14). In response, the CV center decreases

parasympathetic stimulation of the heart by way of motor axons

of the vagus nerves and increases sympathetic stimulation of the

heart via cardiac accelerator nerves. Another consequence of increased sympathetic stimulation is increased secretion of epinephrine and norepinephrine by the adrenal medulla. As the heart

beats faster and more forcefully, and as systemic vascular resistance increases, cardiac output and systemic vascular resistance

rise, and blood pressure increases to the normal level.

Conversely, when an increase in pressure is detected, the baroreceptors send impulses at a faster rate. The CV center responds by

increasing parasympathetic stimulation and decreasing sympathetic stimulation. The resulting decreases in heart rate and force

of contraction reduce the cardiac output. The cardiovascular center

also slows the rate at which it sends sympathetic impulses along

vasomotor neurons that normally cause vasoconstriction. The

resulting vasodilation lowers systemic vascular resistance. Decreased cardiac output and decreased systemic vascular resistance

both lower systemic arterial blood pressure to the normal level.

Moving from a prone (lying down) to an erect position decreases

blood pressure and blood flow in the head and upper part of the

body. The baroreceptor reflexes, however, quickly counteract the

drop in pressure. Sometimes these reflexes operate more slowly

than normal, especially in the elderly, in which case a person can

faint due to reduced brain blood flow after standing up too quickly.



Carotid Sinus Massage

CLINICAL CONNECTION | and Carotid Sinus



Syncope

Because the carotid sinus is close to the anterior surface of the neck,

it is possible to stimulate the baroreceptors there by putting pressure

on the neck. Physicians sometimes use carotid sinus massage, which

involves carefully massaging the neck over the carotid sinus, to slow

heart rate in a person who has paroxysmal superventricular tachycardia, a type of tachycardia that originates in the atria. Anything that

stretches or puts pressure on the carotid sinus, such as hyperextension

of the head, tight collars, or carrying heavy shoulder loads, may also

slow heart rate and can cause carotid sinus syncope, fainting due

to inappropriate stimulation of the carotid sinus baroreceptors. •



Chemoreceptor Reflexes

Chemoreceptors, sensory receptors that monitor the chemical

composition of blood, are located close to the baroreceptors of the

carotid sinus and arch of the aorta in small structures called carotid

bodies and aortic bodies, respectively. These chemoreceptors

detect changes in blood level of O2, CO2, and Hϩ. Hypoxia (lowered O2 availability), acidosis (an increase in Hϩ concentration), or

hypercapnia (excess CO2) stimulates the chemoreceptors to send

impulses to the cardiovascular center. In response, the CV center

increases sympathetic stimulation to arterioles and veins, producing vasoconstriction and an increase in blood pressure. These chemoreceptors also provide input to the respiratory center in the brain

stem to adjust the rate of breathing.



21.4 CONTROL OF BLOOD PRESSURE AND BLOOD FLOW



Hormonal Regulation of Blood Pressure



When blood pressure decreases, heart rate increases.



STIMULUS



Disrupts homeostasis

by decreasing



CONTROLLED CONDITION

Blood pressure



RECEPTORS

Baroreceptors

in carotid sinus

and arch of aorta





Input



Stretch less, which decreases

rate of nerve impulses



CONTROL CENTERS

CV center in

medulla oblongata



Output

Increased

sympathetic,

decreased parasympathetic

stimulation



Adrenal

medulla



Increased secretion

of epinephrine and

norepinephrine

from adrenal medulla



Return to homeostasis

when increased

cardiac output and

increased vascular

resistance bring

blood pressure

back to normal



1. Renin–angiotensin–aldosterone (RAA) system. When blood

volume falls or blood flow to the kidneys decreases, juxtaglomerular cells in the kidneys secrete renin into the bloodstream. In sequence, renin and angiotensin-converting enzyme

(ACE) act on their substrates to produce the active hormone

angiotensin II (anЈ-je¯-o¯-TEN-sin), which raises blood pressure in two ways. First, angiotensin II is a potent vasoconstrictor; it raises blood pressure by increasing systemic vascular

resistance. Second, it stimulates secretion of aldosterone,

which increases reabsorption of sodium ions (Naϩ) and water

by the kidneys. The water reabsorption increases total blood

volume, which increases blood pressure. (See Section 21.6.)

2. Epinephrine and norepinephrine. In response to sympathetic

stimulation, the adrenal medulla releases epinephrine and norepinephrine. These hormones increase cardiac output by increasing the rate and force of heart contractions. They also

cause vasoconstriction of arterioles and veins in the skin and

abdominal organs and vasodilation of arterioles in cardiac and

skeletal muscle, which helps increase blood flow to muscle

during exercise. (See Figure 18.20.)

3. Antidiuretic hormone (ADH). Antidiuretic hormone (ADH)

is produced by the hypothalamus and released from the posterior pituitary in response to dehydration or decreased blood

volume. Among other actions, ADH causes vasoconstriction,

which increases blood pressure. For this reason ADH is also

called vasopressin. (See Figure 18.9.) ADH also promotes

movement of water from the lumen of kidney tubules into the

bloodstream. This results in an increase in blood volume and

a decrease in urine output.

4. Atrial natriuretic peptide (ANP). Released by cells in the atria

of the heart, atrial natriuretic peptide (ANP) lowers blood

pressure by causing vasodilation and by promoting the loss of

salt and water in the urine, which reduces blood volume.

Table 21.2 summarizes the regulation of blood pressure by

hormones.



EFFECTORS

Heart



Autoregulation of Blood Flow



Blood

vessels



Increased stroke

volume and heart rate

lead to increased

cardiac output (CO)



As you learned in Chapter 18, several hormones help regulate blood

pressure and blood flow by altering cardiac output, changing systemic vascular resistance, or adjusting the total blood volume:



Constriction of blood

vessels increases

systemic vascular

resistance (SVR)



RESPONSE

Increased blood pressure



Does this negative feedback cycle represent the changes

that occur when you lie down or when you stand up?



In each capillary bed, local changes can regulate vasomotion.

When vasodilators produce local dilation of arterioles and relaxation of precapillary sphincters, blood flow into capillary networks is increased, which increases O2 level. Vasoconstrictors

have the opposite effect. The ability of a tissue to automatically

adjust its blood flow to match its metabolic demands is called

¯ -shun). In tissues such as the

autoregulation (awЈ-to¯-regЈ-uˉ-LA

heart and skeletal muscle, where the demand for O2 and nutrients

and for the removal of wastes can increase as much as tenfold

during physical activity, autoregulation is an important contributor to increased blood flow through the tissue. Autoregulation

also controls regional blood flow in the brain; blood distribution

to various parts of the brain changes dramatically for different



21



pressure via baroreceptor reflexes.



C H A P T E R



Figure 21.14 Negative feedback regulation of blood



747



748



CHAPTER 21



• THE CARDIOVASCULAR SYSTEM: BLOOD VESSELS AND HEMODYNAMICS



TABLE 21.2



Blood Pressure Regulation by Hormones

FACTOR INFLUENCING

BLOOD PRESSURE



HORMONE



EFFECT

ON BLOOD

PRESSURE



Norepinephrine, epinephrine.



Increase.



CARDIAC OUTPUT

Increased heart rate

and contractility



SYSTEMIC VASCULAR RESISTANCE

Vasoconstriction



Angiotensin II,

antidiuretic hormone

(ADH), norepinephrine,*

epinephrine.†



Increase.



Vasodilation



Atrial natriuretic peptide

(ANP), epinephrine,† nitric

oxide.



Decrease.



Blood volume increase



Aldosterone, antidiuretic

hormone.



Increase.



Blood volume decrease



Atrial natriuretic peptide.



Decrease.



The walls of blood vessels in the systemic circulation dilate in response to low O2. With vasodilation, O2 delivery increases, which

restores the normal O2 level. By contrast, the walls of blood vessels in the pulmonary circulation constrict in response to low levels of O2. This response ensures that blood mostly bypasses those

alveoli (air sacs) in the lungs that are poorly ventilated by fresh air.

Thus, most blood flows to better-ventilated areas of the lung.

CHECKPOINT



13. What are the principal inputs to and outputs from the

cardiovascular center?

14. Explain the operation of the carotid sinus reflex and the

aortic reflex.

15. What is the role of chemoreceptors in the regulation of

blood pressure?

16. How do hormones regulate blood pressure?

17. What is autoregulation, and how does it differ in the

systemic and pulmonary circulations?



BLOOD VOLUME



*Acts at ␣1 receptors in arterioles of abdomen and skin.



Acts at ␤2 receptors in arterioles of cardiac and skeletal muscle; norepinephrine has a much smaller vasodilating effect.



mental and physical activities. During a conversation, for example, blood flow increases to your motor speech areas when

you are talking and increases to the auditory areas when you are

listening.

Two general types of stimuli cause autoregulatory changes in

blood flow:

1. Physical changes. Warming promotes vasodilation, and cooling causes vasoconstriction. In addition, smooth muscle in

arteriole walls exhibits a myogenic response (mı¯-o¯-JEN-ik)—

it contracts more forcefully when it is stretched and relaxes

when stretching lessens. If, for example, blood flow through

an arteriole decreases, stretching of the arteriole walls decreases. As a result, the smooth muscle relaxes and produces

vasodilation, which increases blood flow.

2. Vasodilating and vasoconstricting chemicals. Several types

of cells—including white blood cells, platelets, smooth muscle fibers, macrophages, and endothelial cells—release a wide

variety of chemicals that alter blood-vessel diameter.

Vasodilating chemicals released by metabolically active tissue

cells include Kϩ, Hϩ, lactic acid (lactate), and adenosine

(from ATP). Another important vasodilator released by endothelial cells is nitric oxide (NO). Tissue trauma or inflammation causes release of vasodilating kinins and histamine.

Vasoconstrictors include thromboxane A2, superoxide radicals,

serotonin (from platelets), and endothelins (from endothelial

cells).

An important difference between the pulmonary and systemic

circulations is their autoregulatory response to changes in O2 level.



21.5 Checking Circulation

OBJECTIVE



• Define pulse, and systolic, diastolic, and pulse pressures.



Pulse

The alternate expansion and recoil of elastic arteries after each

systole of the left ventricle creates a traveling pressure wave that

is called the pulse. The pulse is strongest in the arteries closest to

the heart, becomes weaker in the arterioles, and disappears altogether in the capillaries. The pulse may be felt in any artery that

lies near the surface of the body that can be compressed against a

bone or other firm structure. Table 21.3 depicts some common

pulse points.

The pulse rate normally is the same as the heart rate, about 70

to 80 beats per minute at rest. Tachycardia (takЈ-i-KAR-de¯-a;

tachy- ϭ fast) is a rapid resting heart or pulse rate over 100 beats/

min. Bradycardia (bra¯dЈ-i-KAR-de¯-a; brady- ϭ slow) is a slow

resting heart or pulse rate under 50 beats/min. Endurance-trained

athletes normally exhibit bradycardia.



Measuring Blood Pressure

In clinical use, the term blood pressure usually refers to the pressure in arteries generated by the left ventricle during systole and

the pressure remaining in the arteries when the ventricle is in diastole. Blood pressure is usually measured in the brachial artery

in the left arm (Table 21.3). The device used to measure blood

pressure is a sphygmomanometer (sfigЈ-mo¯-ma-NOM-e-ter;

sphygmo- ϭ pulse; -manometer ϭ instrument used to measure

pressure). It consists of a rubber cuff connected to a rubber bulb

that is used to inflate the cuff and a meter that registers the pressure in the cuff. With the arm resting on a table so that it is about

the same level as the heart, the cuff of the sphygmomanometer is

wrapped around a bared arm. The cuff is inflated by squeezing the

bulb until the brachial artery is compressed and blood flow stops,



21.5 CHECKING CIRCULATION



749



TABLE 21.3



Pulse Points

STRUCTURE



LOCATION



STRUCTURE



LOCATION



Superficial temporal artery



Medial to ear.



Femoral artery



Inferior to inguinal ligament.



Facial artery



Mandible (lower jawbone) on line

with corners of mouth.



Popliteal artery



Posterior to knee.



Radial artery



Lateral aspect of wrist.



Common carotid artery



Lateral to larynx (voice box).



Superior to instep of foot.



Brachial artery



Medial side of biceps brachii muscle.



Dorsal artery of foot

(dorsalis pedis artery)



Superficial temporal artery

Facial artery

Common carotid artery

Femoral artery



Popliteal artery



Brachial artery



Radial artery

Dorsal artery of foot

(dorsalis pedis artery)



pressure.

As the cuff is deflated, sounds first occur at the systolic

blood pressure; the sounds suddenly become faint at the

diastolic blood pressure.

140



Pressure in cuff



120

100

80

60



Systolic

blood pressure

(first sound heard)



Diastolic

blood pressure

(last sound heard)



Time



If a blood pressure is reported as “142 over 95,” what

are the diastolic, systolic, and pulse pressures? Does

this person have hypertension as defined in Disorders:

Homeostatic Imbalances at the end of the chapter?



C H A P T E R



Figure 21.15 Relationship of blood pressure changes to cuff



21



(open) ductus arteriosus greatly increase pulse pressure. The normal ratio of systolic pressure to diastolic pressure to pulse pressure

is about 3:2:1.



Pressure (mmHg)



about 30 mmHg higher than the person’s usual systolic pressure.

The technician places a stethoscope below the cuff on the brachial

artery, and slowly deflates the cuff. When the cuff is deflated

enough to allow the artery to open, a spurt of blood passes through,

resulting in the first sound heard through the stethoscope. This

sound corresponds to systolic blood pressure (SBP), the force of

blood pressure on arterial walls just after ventricular contraction

(Figure 21.15). As the cuff is deflated further, the sounds suddenly become too faint to be heard through the stethoscope. This

level, called the diastolic blood pressure (DBP), represents the

force exerted by the blood remaining in arteries during ventricular

relaxation. At pressures below diastolic blood pressure, sounds

disappear altogether. The various sounds that are heard while taking blood pressure are called Korotkoff sounds (ko¯-ROT-kof).

The normal blood pressure of an adult male is less than 120 mmHg

systolic and less than 80 mmHg diastolic. For example, “110 over 70”

(written as 110/70) is a normal blood pressure. In young adult

females, the pressures are 8 to 10 mmHg less. People who exercise regularly and are in good physical condition may have even

lower blood pressures. Thus, blood pressure slightly lower than

120/80 may be a sign of good health and fitness.

The difference between systolic and diastolic pressure is called

pulse pressure. This pressure, normally about 40 mmHg, provides information about the condition of the cardiovascular system. For example, conditions such as atherosclerosis and patent



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